Growth Hormone Deficiency During the Transition Phase

The transition period is the span of time in which people complete their somatic and psychological development after reaching their full stature (also known as late teenage years, post-adolescence or young adulthood). It starts in late puberty and comes to an end at around 25 years of age, thus lasting from three to 10 years. It includes hormonal and many lifestyle changes that lead to a different perception of the self and one’s capacity to relate to others.

The transition period is the span of time in which people complete their somatic and psychological development after reaching their full stature (also known as late teenage years, post-adolescence or young adulthood). It starts in late puberty and comes to an end at around 25 years of age, thus lasting from three to 10 years. It includes hormonal and many lifestyle changes that lead to a different perception of the self and one’s capacity to relate to others. There is also a change in the mental and physical needs of patients with growth hormone deficiency (GHD) who are leaving childhood to become adolescents and then young adults.^1,2

Peak bone mass and complete reproductive maturation (demonstrated, in males, by the refinement of semen parameters) are achieved in the transition period. As confirmed by the literature over the last decade, the growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis is essential to achieve optimal body composition and bone density and maintain a safe metabolic profile (thereby decreasing cardiovascular risk). It also has a generally positive influence onquality of life. Normally, recombinant GH (rec-GH) therapy is administered to GH-deficient children to enable them to achieve a satisfactory height, the main target for this period of life. However its use is now accepted and recognised for patients entering the transition period who were GH-deficient during childhood and adolescence, given these other important effects.^7,8 It should also be considered if there is a possibility of youth-onset GHD (e.g. following a road accident), which is presumably more difficult to diagnose and would generate less concern, especially if final height had already been reached. Given this, a retest during the transition period is essential, in order to evaluate if there is still a GH-deficiency and if a replacement therapy is still required. It is useful to comment briefly that GH is a polypeptide hormone produced by somatotrope cells of the adenohypophysis: its release is stimulated by growth hormone-releasing hormone (GHRH) produced by the hypothalamus, and inhibited by somatostatin. GH does not work alone, but has a peripheral effector known as IGF-1 due to its structural similarity with insulin. IGF-1 is produced by the liver under GH stimulation and is the substance that actually interacts with peripheral tissues.

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